Mitochondrial function are involved in the toxicity of many xenobiotic compounds (A chemical compounds foreign to a living organism). We are increasingly exposed to a variety of xenobiotic compounds such as drugs, environmental pollutants, and even naturally produced toxins. The toxicity of many of these compounds involves either direct or secondary effects on mitochondrial function. Examples of direct effects include inhibition of electron transport system components that can disrupt energy production and lead to oxidative stress. Indirect effects can occur through stimulation of non-mitochondrial oxidative stress that then results in impaired mitochondrial function and amplification of the toxicity. The acute toxicity effects of high dose exposures of many compounds are well established. However, the mechanisms by which chronic exposure disrupts cell and organismal function and contributes to lasting dysfunction are less well known. Our lab is particularly interested in the interaction between mitochondrial biology, chronic xenobiotic exposure, and disease. We are pursuing this area in collaboration with toxicologists and clinical scientists.